Smoking cessation treatment for COPD smokers: the role of counselling

Smoking cessation is the only therapeutic intervention that can prevent COPD smokers from the chronic progression of their disorder. The most important intervention for helping these smokers to quit is a combination of counseling plus pharmacological treatment. The characteristics of the counseling should be different depending if this intervention is offered to smokers with a previous diagnosis of COPD or if the intervention is offered to smokers who have been recently diagnoses with COPD. The counseling of patients who have been recently diagnosed should include: a) explanation of the direct relationship between smoking and COPD, b) encouraging these patients to quit and c) using of spirometry and measurements of CO as a motivational tools. The counseling of patients who have been previously diagnosed should include: a) encouragement to make a serious quit attempt, b) an intervention that increases motivation, self-efficacy and self-esteem, c) and the intervention should also control depression and be directed to weight gain control

Supplementary Material for: Predictors of Success for Smoking Cessation at the Workplace: A Longitudinal Study

<b><i>Background:</i></b> The effectiveness of worksite interventions to reduce smoking is debatable. <b><i>Objectives:</i></b> A<b> </b>comprehensive smoking cessation intervention was implemented in a community of more than 17,000 employees at three different health care companies. The primary endpoint was abstinence at 24 months (self-reported and confirmed by exhaled carbon monoxide ≤6 parts per million). Predictors of long-term abstinence were analysed by multivariable regression analysis. <b><i>Methods:</i></b> The study was designed as an investigator-initiated and investigator-driven, open, multicentre, cohort study; 887 smokers<b> </b>were enrolled in the programme. The intervention included intensive individual counselling as well as nicotine replacement and/or bupropion according to individual preferences. Re-interventions for relapse were offered during the 24-month follow-up. <b><i>Results:</i></b> The abstinence rate was 37% at 24 months and did not differ among the various medication groups (p > 0.05 for all). Predictors of successful cessation were higher age (odds ratio, OR 1.47, 95% confidence interval, CI 1.08-2.00, p < 0.01), breathlessness on exertion (OR 2.26, 95% CI 1.1-4.9, p = 0.03), and a higher educational level (OR 1.81, 95% CI 1.06-3.09, p = 0.03). Higher Fagerström (OR 0.76, 95% CI 0.59-0.97, p < 0.01) and craving scores (OR 0.75, 95% CI 0.63-0.89, p < 0.01), chronic sputum production (OR 0.52, 95% CI 0.31-0.87, p = 0.01) and use of antidepressants (OR 0.54, 95% CI 0.32-0.91, p = 0.02) were associated with ongoing smoking. <b><i>Conclusion:</i></b> A<b> </b>comprehensive smoking cessation intervention at the workplace achieves high, stable, long-term abstinence rates. Elderly, well-educated employees with breathlessness on exertion have higher odds of quitting smoking. In contrast, those with high physical dependency and more intense craving, and those reporting use of antidepressant medication or sputum production have poorer chances to quit

The Influence of Chronic Cigarette Smoking on Neurocognitive Recovery after Mild Traumatic Brain Injury

The majority of the approximately 1.7 million civilians in the United States who seek emergency care for traumatic brain injury (TBI) are classified as mild (MTBI). Premorbid and comorbid conditions that commonly accompany MTBI may influence neurocognitive and functional recovery. This study assessed the influence of chronic smoking and hazardous alcohol consumption on neurocognitive recovery after MTBI. A comprehensive neurocognitive battery was administered to 25 non-smoking MTBI participants (nsMTBI), 19 smoking MTBI (sMTBI) 38±22 days (assessment point 1: AP1) and 230±36 (assessment point 2: AP2) days after injury. Twenty non-smoking light drinkers served as controls (CON). At AP1, nsMTBI and sMTBI were inferior to CON on measures of auditory-verbal learning and memory; nsMTBI performed more poorly than CON on processing speed and global neurocognition, and sMTBI performed worse than CON on working memory measures; nsMTBI were inferior to sMTBI on visuospatial memory. Over the AP1-AP2 interval, nsMTBI showed significantly greater improvement than sMTBI on measures of processing speed, visuospatial learning and memory, visuospatial skills, and global neurocognition, whereas sMTBI only showed significant improvement on executive skills. At AP2, sMTBI remained inferior to CON on auditory-verbal learning and auditory-verbal memory; there were no significant differences between nsMTBI and CON or among nsMTBI and sMTBI on any domain at AP2. Hazardous alcohol consumption was not significantly associated with change in any neurocognitive domain. For sMTBI, over the AP1-AP2 interval, greater lifetime duration of smoking and pack-years were related to significantly less improvement on multiple domains. Results suggest consideration of the effects of chronic cigarette smoking is necessary to understand the potential factors influencing neurocognitive recovery after MTBI